My main research interest, the evolution of human cognition, grew from a particular interest in the mental processes underpinning social behaviour, language and moral reasoning. The selective pressures acting on a trait co-evolve with the mechanisms of heritability operating. One such mechanism, uncovered in the 1980s, has radically impacted our understanding of nature and nurture: ‘genomic imprinting represents a paradigm shift in genetics comparable to the Einsteinian revolution in physics’ (Goshen et al., 1994) The study of epigenetic mechanisms such as genomic imprinting drives the developing field of gene-environment interaction which is central to explaining one of the major conundrums in evolutionary psychology: how selection could produce the plasticity of the human mind.
This is a question in evolutionary anthropology rather than molecular genetics, and requires an analysis of phenotypes, i.e. traits, since selection acts on phenotypes not genes. In order for imprinting to act on phenotypes in such a way that selection can act, the effect of imprinting must be discernible in the phenotype, as traits, i.e. the effect must be measurable. Autistic spectrum condition (AC) appears to be influenced by imprinting and has also been modelled as an extreme phenotype otherwise continuous with the normal population. This suggests that the influence of imprinting on the normal range of behaviours can be assessed using measures developed from the study of AC.
My PhD focused on the influence of imprinted genes (i.e. preferentially expressed from one parent) on the evolution of social cognition and executive function by looking for parent-of-origin effects on autistic spectrum traits (empathy and systemizing) and behavioural inhibition and activation in the general population. The results suggest a modification of the evolutionary ‘Conflict Hypothesis’ and more recent ‘Imprinted Brain Hypothesis’ which pit maternal and paternal interests against each other in an escalating power struggle via imprinted genes. This modification could be termed ‘Conspiracy out of Conflict’ and has greater explanatory power.
My research aims to extend this work within the framework of the adaptive mind facilitated by gene-environment interaction, such as the epigenetic regulation of mental traits in response to environmental cues: nature via nurture. This involves, for example, defining the target phenotypes in a biologically meaningful way. I am particularly interested in empathy and theory of mind. The success of genetic linkage studies depends on how the phenotype has been defined.
I am also looking at how to analyse pedigree data to detect the influence of imprinted genes. Generating theoretical data has tremendous potential for further refining the model fitting process (since imprinting models are more complicated to fit, e.g. using structural equation modelling, than classical models). This kind of model fitting could also be applied to appropriate existing datasets as collaborative projects.
I also teach a couple of biology-oriented psychology courses with the Open University, UK.
Contact Gill at firstname.lastname@example.org